properties of cardiac muscle - linn–benton community...

3/1/2016

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Part 2

The Cardiovascular System

• Cardiac muscle

–Striated

–Short

–Wide

–Branched

–Interconnected

• Skeletal muscle

–Striated

–Long

–Narrow

–Cylindrical

Properties of cardiac muscle

• Cells connected to each other by intercalated discs

– Passage of ions between cells

– Allows entire heart to work as a syncytium

• Numerous large mitochondria

–25–35% of cell volume

–Increases cell capacity to do what?

• Able to utilize many food molecules

–Example: lactic acid

–Most cells primarily use what?

Properties of Cardiac Muscle

Figure 18.11a

Nucleus

DesmosomesGap junctions

Intercalated discs Cardiac muscle cell

(a)

Figure 18.11b

Nucleus

Nucleus

I bandA band

Cardiac

muscle cell

Sarcolemma

Z disc

Mitochondrion

Mitochondrion

T tubule

Sarcoplasmic

reticulum

I band

Intercalated

disc

(b)

• Some cells are myogenic

– Contractile impulse originates in non-contractile pacemaker cells,

not in nerve cells

• Cardiac control center in medulla can increase or decrease rate

through ANS

• Primary innervation is inhibitory through vagus nerve

– Sympathetic or PNS?

–Because cells are joined by gap junctions, spontaneous

depolarization of pacemaker cells initiates depolarization of

contractile cells too


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• Heart contracts as a unit or not at all (video)

–Sodium channels leak slowly in specialized cells

• Spontaneous depolarization

• Leakage rate sets rhythm

–Compare to skeletal muscle


Figure 18.13

1 2 3Pacemaker potential

This slow depolarization is

due to both opening of Na+

channels and closing of K+

channels. Notice that the

membrane potential is

never a flat line.

Depolarization The

action potential begins when

the pacemaker potential

reaches threshold.

Depolarization is due to Ca2+

influx through Ca2+ channels.

Repolarization is due to

Ca2+ channels inactivating and

K+ channels opening. This

allows K+ efflux, which brings

the membrane potential back

to its most negative voltage.

Action

potential

Threshold

Pacemaker

potential

1 1

2 2

3

Action Potential in Myogenic Cells of the Heart

Figure 18.12

Absolute

refractory

period

Tension

development

(contraction)

Plateau

Action

potential

Time (ms)

1

2

3

Depolarization is

due to Na+ influx through

fast voltage-gated Na+

channels. A positive

feedback cycle rapidly

opens many Na+

channels, reversing the

membrane potential.

Channel inactivation ends

this phase.

Plateau phase is

due to Ca2+ influx through

slow Ca2+ channels. This

keeps the cell depolarized

because few K+ channels

are open.

Repolarization is

due to Ca2+ channels

inactivating and K+

channels opening. This

allows K+ efflux, which

brings the membrane

potential back to its

resting voltage.

1

2

3

Tensio

n (

g)

Me

mb

ra

ne

po

ten

tia

l (m

V)

Action Potential of Contractile Cardiac Muscle Cells

Allows sufficient refilling

of the heart before the next beat

• Terms

– Systole

• Contraction of ventricles

– Diastole

• Relaxation of ventricles

Conduction System of the Heart

• Specialized cardiac cells

– Initiate impulse

– Conduct impulse


SA node (pacemaker)

Atrial depolarization and contraction

AV node

Bundle of His

Right and left bundle branches

Purkinje fibers

Myocardium

Contraction of ventricles

Conduction system of the heart

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1. Sinoatrial (SA) node (pacemaker)

– Generates impulses about 70-75 times/minute (sinus rhythm)

– Depolarizes faster than any other part of the myocardium

– Cut the vagus nerve = HR immediately increases by ~25bpm

2. Atrioventricular (AV) node

– Delays impulses approximately 0.1 second

– Depolarizes 50 times per minute in absence of SA node input


3. Atrioventricular (AV) bundle (bundle of His)– Only electrical connection between the atria and

ventricles

4. Right and left bundle branches– Two pathways in the interventricular septum that

carry the impulses toward the apex of the heart

5. Purkinje fibers– Complete the pathway into the apex and ventricular

walls

Conduction system of the heart

Figure 18.14a

(a) Anatomy of the intrinsic conduction system showing the

sequence of electrical excitation

(Intrinsic Innervation)

Internodal pathway

Superior vena cava

Right atrium

Left atrium

Purkinje

fibers

Inter-

ventricular

septum

1 The sinoatrial (SA)

node (pacemaker)

generates impulses.

2 The impulses

pause (0.1 s) at the

atrioventricular

(AV) node.

The atrioventricular

(AV) bundle

connects the atria

to the ventricles.

4 The bundle branches

conduct the impulses

through the

interventricular septum.

3

The Purkinje fibers

depolarize the contractile

cells of both ventricles.

5

Conduction Pathway

• Intrinsic innervation

• External influences

• Normal:

– Average = 70 bpm

– Range = 60-100 bpm

Conduction System of the heart

Figure 18.15

Thoracic spinal cord

The vagus nerve (parasympathetic) decreases heart rate.

Cardioinhibitory center

Cardio-

acceleratory

center

Sympathetic cardiacnerves increase heart rateand force of contraction.

Medulla oblongata

Sympathetic trunk ganglion

Dorsal motor nucleus of vagus

Sympathetic trunk

AV node

SA nodeParasympathetic fibers

Sympathetic fibers

Interneurons

• Sympathetic stimulation

– Enhances Ca2+ movement in contractile cells

– Increases HR, contractility

• Stroke volume decreases due to less ventricular filling time

– Speeds relaxation


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• Parasympathetic stimulation

– Dominant signal under resting conditions

– Cardiac response mediated by acetylcholine

– Opens K+ channels, hyperpolarizes cells

– Decreases HR

– Innervation of ventricles is sparse = little effect on contractility


• Other influences

– Blood pressure

– Atrial reflex

• Increased rate of blood returning to heart -> atrial stretching ->

increased HR

– Hormonal

• Epinephrine, thyroxine = increase HR

– Ion balance

– Exercise

– Temperature

– Exercise

– Age


Defects in the intrinsic conduction system may

result in

1. Arrhythmias: irregular heart rhythms

2. Bradycardia < 60 bpm

3. Tachycardia >100 bpm

4. Maximum is about 300 bpm

Homeostatic Imbalances

• A composite of all the action potentials generated by nodal

and contractile cells at a given time

– Represents movement of ions = bioelectricity

– Three waves

1. P wave: electrical depolarization of atria

2. QRS complex: ventricular depolarization

3. T wave: ventricular repolarization

Electrocardiography

Figure 18.16

Sinoatrial

node

Atrioventricular

node

Atrial

depolarization

QRS complex

Ventricular

depolarization

Ventricular

repolarization

P-Q

Interval

S-T

Segment

Q-T

Interval

Figure 18.17

Atrial depolarization, initiatedby the SA node, causes theP wave.

P

R

T

QS

SA node

AV node

With atrial depolarizationcomplete, the impulse isdelayed at the AV node.

Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.

P

R

T

QS

P

R

T

QS

Ventricular depolarizationis complete.

Ventricular repolarizationbegins at apex, causing theT wave.

Ventricular repolarizationis complete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization Repolarization

1

2

3

4

5

6

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Figure 18.18

(a) Normal sinus rhythm.

NORMAL HEART RHYTHM

Figure 18.18

(b) Junctional rhythm. The SA

node is nonfunctional, P waves

are absent, and heart is paced by

the AV node at 40 - 60 beats/min.

ARRHYTHMIAS

Figure 18.18

(c) Second-degree heart block.

Some P waves are not conducted

through the AV node; hence more

P than QRS waves are seen. In

this tracing, the ratio of P waves

to QRS waves is mostly 2:1.

ARRHYTHMIAS

Figure 18.18

(d) Ventricular fibrillation. These

chaotic, grossly irregular ECG

deflections are seen in acute

heart attack and electrical shock.

ARRHYTHMIAS

Video

Atrial fibrillation . Rapid, irregular heartbeat. Note the

absence of P waves (which represent depolarization of

the top of the heart)

ARRHYTHMIAS

Atrial

fibrillation

Normal

Normal Atrial fibrillation

ARRHYTHMIAS

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• All events associated with blood flow through the heart

during one complete heartbeat

–Systole— ventricular contraction (ejection of blood)

–Diastole— ventricular relaxation (receiving of

blood)

The Cardiac Cycle

• Three events

1) Recordable bioelectrical disturbances (EKG)

2) Contraction of cardiac muscle

3) Generation of pressure and volume changes

• Blood flows from areas of higher pressure to areas of lower

pressure

– Valves prevent backflow

The Cardiac Cycle

• Ventricular filling → ventricular systole

– Backpressure closes AV valves = isovolumetric

contraction

– Ventricular pressure becomes greater than aorta &

pulmonary artery pressure = semilunar valves open

• Portion of ventricular contents ejected

The cardiac cycle

Figure 18.20

1 2a 2b 3

Atrioventricular valves

Aortic and pulmonary valves

Open OpenClosed

Closed ClosedOpen

Phase

ESV

Left atrium

Right atrium

Left ventricle

Right ventricle

Ventricular

filling

Atrial

contraction

Ventricular filling

(mid-to-late diastole)

Ventricular systole

(atria in diastole)

Isovolumetric

contraction phase

Ventricular

ejection phase

Early diastole

Isovolumetric

relaxation

Ventricular

filling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRS

P

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Ventric

ula

r

volu

me (

ml)

Pressure (

mm

Hg)

EKG

Pressure

changes

Changes in

volume

Contraction

Control of blood flow

• Two sounds associated with closing of heart valves

–First sound occurs as AV valves close and signifies

beginning of systole = Lub

–Second sound occurs when SL valves close at the

beginning of ventricular diastole = Dub

• Heart murmurs = abnormal heart sounds

– Most often indicative of valve problems

Heart Sounds

Figure 18.19

Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space

Aortic valve sounds heard in 2nd intercostal space atright sternal margin

Pulmonary valvesounds heard in 2ndintercostal space at leftsternal margin

Mitral valve soundsheard over heart apex(in 5th intercostal space)in line with middle ofclavicle

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Figure 18.20

1 2a 2b 3



Open OpenClosed

Closed ClosedOpen

Phase

ESV

Left atrium

Right atrium

Left ventricle

Right ventricle

Ventricular

filling

Atrial

contraction

Ventricular filling


Ventricular systole

(atria in diastole)

Isovolumetric

contraction phase

Ventricular

ejection phase

Early diastole

Isovolumetric

relaxation

Ventricular

filling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRS

P

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Ventric

ula

r

volu

me (

ml)

Pressure (

mm

Hg)

Pressure

changes

Changes in

volume

• Mitral stenosis

Heart Sounds

• Valvular insufficiency (regurgitation)

Heart sounds

• Example: mitral valve prolapse

Heart Sounds

• Definition: volume of blood pumped by each ventricle in one

minute

– AKA: Minute volume

• 2 major factors

– Stroke volume (SV)

– Heart rate (HR)

Cardiac Output (CO)

• CO (ml/min) = heart rate (HR) x stroke volume (SV)

–HR = number of beats per minute

–SV = volume of blood pumped out by a ventricle with

each beat (ml/min)

Cardiac output

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• Stroke volume

– Difference between EDV and ESV

• EDV-ESV=SV

– Average is about 75 ml

Cardiac output

Figure 18.20

1 2a 2b 3



Open OpenClosed

Closed ClosedOpen

Phase

ESV

Left atrium

Right atrium

Left ventricle

Right ventricle

Ventricular

filling

Atrial

contraction

Ventricular filling


Ventricular systole

(atria in diastole)

Isovolumetric

contraction phase

Ventricular

ejection phase

Early diastole

Isovolumetric

relaxation

Ventricular

filling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRS

P

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Ventric

ula

r

volu

me (

ml)

Pressure (

mm

Hg)

EKG

Pressure

changes

Changes in

volume

• At rest

–CO (ml/min) = HR (75 beats/min) × SV (70 ml/beat)

= 5.25 L/min

– Maximal CO is 4–5 times resting CO in nonathletic people

– CO may reach 30 L/min in trained athletes

– Cardiac reserve

• Difference between resting and maximal CO

Cardiac Output (CO)

• Stroke volume

– Three main factors affect SV

• Preload

• Contractility

• Afterload

Regulation of stroke volume

• Preload

– Frank-Starling law of the heart: the heart can change its CO

according to the incoming volume of blood

• At rest, cardiac muscle cells are shorter than optimal length

• Must be a degree of stretch of cardiac muscle cells before they contract

–Slow heartbeat and exercise increase venous return

–Increased venous return distends (stretches) the ventricles

and increases contraction force

Regulation of Stroke Volume Regulation of Stroke Volume

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• Contractility

– Contractile strength at a given muscle length, independent of muscle stretch and EDV

• Agents increasing contractility

– Increased Ca2+ influx

» Sympathetic stimulation

– Hormones

» Thyroxin, glucagon, and epinephrine

• Agents decreasing contractility

– Calcium channel blockers

Regulation of Stroke Volume

Increase SV

Decrease ESV

• Afterload

– Pressure (resistance) that must be overcome for ventricles to eject

blood

• Hypertension increases afterload

– Results in increased ESV and reduced SV

Regulation of Stroke Volume

• Sympathetic nervous system

–Norepinephrine

• Increased SA node firing rate

• Faster conduction through AV node

• Increases excitability of heart by increasing Ca2+ availability

• Parasympathetic nervous system

– Vagus nerve

• Decreases HR

Who dominates at rest?

Control of Heart rate

Figure 18.22

Venousreturn

ContractilitySympathetic

activityParasympathetic

activity

EDV(preload)

Strokevolume

Heartrate

Cardiacoutput

ESV

Exercise (byskeletal muscle andrespiratory pumps;

see Chapter 19)

Heart rate(allows more

time forventricular

filling)

Bloodborneepinephrine,

thyroxine,excess Ca2+

Exercise,fright, anxiety

Initial stimulus

Result

Physiological response

Figure 18.15

Thoracic spinal cord

The vagus nerve (parasympathetic) decreases heart rate.

Cardioinhibitory center

Cardio-

acceleratory

center

Sympathetic cardiacnerves increase heart rateand force of contraction.

Medulla oblongata

Sympathetic trunk ganglion

Dorsal motor nucleus of vagus

Sympathetic trunk

AV node

SA nodeParasympathetic fibers

Sympathetic fibers

Interneurons

• Other factors…

Control of heart rate

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Cardiac Output

Cardiac output

Stroke volumeHeart rate

Usually set by SA

node

Preload Contractility Afterload

Rate of venous

return

Ca2+, hormones Blood pressureAutonomic

nervous system

(among other things)

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